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Esa 3 > Respiration > Flashcards

Respiration Flashcards

0
Q

Define tidal volume, respiratory rate and pulmonary ventilation rate

A

Tidal volume = normal volume expired on a breath (not forced)
Respiratory rate = breaths per minute
Pulmonary ventilation rate = air in and out in one minute = tidal volume x rr

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1
Q

States boyles law, Charles law and the universal gas law

A

Boyles law = pressure is inversely proportional to volume.
Charles law = pressure is directly proportional to temperature
Universal gas law= pressure x vol = temperature x gas constant

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2
Q

What is a meatus?

A

Channel formed by nasal conchae (turbinates) superior middle and inferior.

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3
Q

Define partial pressure, vapour pressure, tension and saturation vapour pressure.

A

Partial pressure - pressure (number of collisions of gas against a container) of just one gas in a mixture.
Vapour pressure - partial pressure of water above a surface of water
Tension - a gases’ tendency to escape a liquid
Saturation vapour pressure - the maximum pressure of water vapour in equilibrium with the liquid phase. Depends on temperature.

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4
Q

What is an olfactory region?

A

Region without as much mucous secretions for smell. Thick epithelia. Washed by serous secretions. Non olfactory have venous sinuses in LP that swell so that air only goes through 1/2 of nose

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5
Q

Describe 4 para nasal sinuses and their use

A

Sphenoidal
Ethmoidal
Maxillary
Frontal

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6
Q

Composition of glottis

A 
Plicae vocales (true) attached to the arytenoid cartilage (posterior to larynx and thyroid cartilage and superior to cricoid cartilage)
Vestibular folds (false)
In between in the rima glottidis
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7
Q

Cartilage in lower respiratory tract?

A

Trachea C shaped and fibroelastic membrane with trachealis.
Primary bronchi - ring
Secondary and tertiary have a crescent, plates or islands
Bronchioles - none

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8
Q

Upper and lower and resp portion?

A

Sternal angle/ glottis

Bronchioles to alveoli.

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9
Q

Describe differences in ribs

A

1atypical - only have inferior facet on head, shortest, broadest, most curved.
2 atypical - no prominent costal groove
3-8- typical
9-10 typical but fuse to costal cartilage which joins costal cartilage of rib above not the sternum.
11-12 atypical ribs don’t fuse to cartilage, lie in diaphragm, only superior facet present on head, no tubercle

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10
Q

Describe the structure of a rib and it’s articulations

A

Head, superior and inferior facets (articulate with Demi facets of vertebral bodies) separated with crest
Neck - tubercule inferior laterally which articulates with transverse facet of vertebrae. (Costotransverse joint)
Costal groove found inferior, arteriorly

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11
Q

What is the costal margin?

A

Where costal cartilages form a V towards the sternum

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12
Q

Describe the intercostal muscles function and innervation.

A

External (anterior and inferior), hands in pockets, raises ribs, inspiration
Internal (anteriorly) and innermost(laterally), 90 deg, depresses ribs, forced expiration.
Supplied by anterior rami of corresponding nerve

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13
Q

Describe the structure of the diaphragm

A

Muscle ribs start from ribs, arcuate ligaments (median, lateral and medial) ad right and left Cruz and go to the central tendon.

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14
Q

Describe the distribution of intercostal nerves arteries and veins and their roots and what the nerves supply. Including supply and drainage

A

Artery- anastomoses between aorta and internal thoracic artery.
Vein - drains into azygous vein (SVC) (some into internal thoracic vein)
Nerve - anterior rami, supplies muscles, skin and costal and cervical parietal pleura.
Found in costal groove and just superior to rib

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15
Q

Phrenic nerve innervation.

A

3,4,5

Diaphragm, sensory to mediastinal and diaphragmatic pleural and the pericardium. Both surfaces of diaphragm.

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16
Q

Describe the pleural cavity and the lines of pleural reflection

A

Costal, cervical, diaphragmatic and mediastinal

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17
Q

Describe the mediastinal and their contents

A

Superior mediastinum. Bounded superiorly by thoracic inlet, inferiorly by T4- angle of Louis/ pericardium. Contains oesophagus, tachea, muscles, phrenic nerve, deep and superior cardiac plexuses, arch of the aorta, thymus, SVC, vagus, muscles
Anterior mediastinum - chest wall and fibrous pericardium. Thymus in kiddies, long thoracic vein and artery, sternophrenic ligament
Posterior mediastinum - descending/thoracic aorta, azygous vein, oesophagus, thoracic duct, vagus nerve, splanchnic nerve, sympathetic veins and trunk

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18
Q

Locations of PV, PA and bronchus in right and left hilum

A 
Bronchi anterior
Veins posterior 3/2
Left artery superior
Right arteries (2) middle
Lymph nodes between veins
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19
Q

What is the rate of diffusion in the lungs usually limited by?

A

Not area, or pressure, diffusion barrier - 5 layers

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20
Q

Describe the properties of the mechanical system comprising the lungs, chest wall and diaphragm

A

Lungs: elastic tissues for recoil
Chest wall: draws chest out via pluera to increase AP
Diameter: contracts to draw chest down increasing sup/infer

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21
Q

Muscles in forced inhalation and expiration?

A

Inspiration: external costal, diaphragm, serratus anterior, pec minor, scalene, sternocleidomastoid
Expiration: innermost and internal intercostal muscles, abdominal muscles

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22
Q

Define functional residual capacity, residual volume, vital capacity and inspiratory capacity

A

Tidal vol - total volume breathed in and out on a normal breath/ displaced with no extra effort.
Inspiratory reserve vol- extra volume than can be inspired than normal
Exploratory reserve vol - extra vol that can be expired than normal
Inspiratory capacity - total amount that can be inhaled after a normal exhale.
Residual vol - air left in lungs after a forced expiration
Functional residual capacity- air left in lungs after a normal expiration
Vital capacity- maximal amount that can be inhaled from the RC

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23
Q

Serial dead space, physiological dead space and how these variables are measured

A

Serial dead space= non collapsible structures- bronchi upwards. Air in structures that do not take part in gas exchange - 150ml. (Conducting airway)

Measured via nitrogen washout, forced expiration, forced inspiration of 100% O2, amount of N2 measured and use to calculate volume.

Physiological dead space= serial dead space + alveolar dead space (gas in alveoli that can’t take place in gas exchange).
Looking at pO2 and pCO2 breathed out compared with normal alveolar pressures as alveolar air is dilated by dead space air.

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24
Q

What is alveolar ventilation rate and how is it calculated?

A

Tidal volume - physiological dead space * respiratory rate

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25
Q

Define compliance of the lungs and how it is measured

A

Stretchiness of lung, higher means more stretch.

Change in vol/ change in pressure

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26
Q

Factors which affect compliance

A

Surface area. As surface area increases then compliance decreases. This is due to water tension.
Surfactants decrease water tension so increase compliance

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27
Q

What is hysteresis?

A

No all energy put into stretching lungs on inspiration is released on recoil. Greatest when tidal vol is maximal.

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28
Q

Why do big bubbles eat little bubbles? (Or not)

A

Laplaces law = 2x SA/ radius = pressure
High bubbles have a lower pressure so eat small bubbles.
Surfactant decreases water tension so bub les are stabalised- less in big bubbles so a higher tension.

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29
Q

Factors which affect airway resistance and how resistance changes over a breathing cycle.

A

Poiseulles law. Resistance through a tube is inversely proportional to radius. Larger radius then lower resistance. Tubes narrow on expiration so more resistance. Compliance also affects how much we can inhale.

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30
Q

Describe spirometry

A

Measures FVC. Can link to a vitalograph to measure over time.
Limited by compliance, for e of muscles and airway resistance

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31
Q

Describe FVC and FEV1.0

A

Force vital capacity and forced expiratory vol in one second

On vitalograph

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32
Q

Explain obstructive and restrictive patterns of spirometry.

A

Obstructive then lower fev e.g. Asthma

Resistrictive the lower FVC e.g. Fibrosis and chest wall probs

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33
Q

Explain inspiratory and expiratory flow volume loops and how they are affected by upper and lower airway obstructions

A

Peak flow meter
PEFR
Decrease in flow after peak flow (at higher vols) unless severe.

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34
Q

Describe the measurement of residual volume

A

Helium dilation - not taken into blood stream. Measure difference in conc.

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35
Q

Describe the measurement of transfer factor.

A

CO, only limited by diffusion barrier. Binds to haem readily. Measure differnces in conc for TF

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36
Q

State the solubility of O2 in body fluid

A

0.01mmol/l/kPA at 37

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37
Q

What are the normal values of alveolar and capillary pO2?

A

13.3

5kPa

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38
Q

Properties of haemoglobin that makes it good

A 
Tetromer. Exists in two states.
Tense hard to bind
Relaxed easy to bind
More PO2 then more R
Highly reversible.
Lower O2 at tissues so more delievered.
High temp and H+ cause more T
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39
Q

Effects on the dissociate curve of a high temp/ fall in pH

A

Right left, harder to bind

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40
Q

Estimate rate of delivery of O2 to tissues at different capillary pO2s and pHs

A

Haem found at 2.2 mmol/ l and bind 4 O2.

Use graph and O2 saturation at different pressures

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41
Q

Factors affecting gas diffusion in alveoli

A

Thickness of barrier/ resistance to diffusion
Partial Pressure gradient
Area

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42
Q

How is the transfer factor obtained/ diffusion capacity

A

Vital capacity containing CO. Exhale, how much CO is there now? pCO in blood =0 and so all that can transfer will have. First 750ml is discarded. Helium used to measure dilution effects.

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43
Q

Reactions of CO2 in blood

A

CO2+H20 = HCO3 + H
In mito, more HCO3 produced so equilibrium to left.
Dissolved CO2 affects pH

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44
Q

What is the Henderson hasselbach equation a and calculate pH given pCO2 and HCO3

A

PH= pK (6.1) + log( HCO3/(CO2*0.23))

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45
Q

Factors affecting HCO3 conc

A

H+ reacts with haemoglobin so more HCO3 produced and leaves RBC via AE
Kidney maintain long term via reabsoption

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46
Q

Buffering action of haem in RBC

A

High CO2 then H+ binds to HCO3 and haem

Low CO2 then Co2 reacts with H2O to form more H+/ dissociates from haem

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47
Q

Function of carb amino proteins

A

Binds to CO2 so that it cannot dissolve. This co2 therefore has no effect on pH. Transport molecules

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48
Q

Normal content of CO2 in arterial and venous blood

A

21.5mmol/l in arterial
23.5 mmol/l in venous
Haem can bind more H+ without O2 in venous so blood can carry more CO2 without pH changing

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49
Q

State the proportion of CO2 travelling in various forms.

A

80% HCO3
11% carbamino
8% dissolves CO2

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50
Q

Define hypoxia hypocapnia, hyperventilation and hypoventilation

A

PCO2<8
Low CO2 (3.5?)
RR 12-20

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51
Q

Effects on plasma pH of hypo and hyper ventilation and the result

A

Effects co2, effects pH.
Acidosis- coma, seizures, arrhythmias, vomiting, nausea
Alkalosis- fainting, dizziness, coma, free Ca decrease so tetany

52
Q

Define respiratory acidosis and alkalosis, compensated respiratory acidosis and alkalosis

A

Due to over/ under ventilation/perfusion rise/fall in CO2 so pH effects.
Compensated by kidney- removal of HCO3 or retention

53
Q

Define metab acid/alk and compensated?

A

Due to metabolic cause e.g. Ketoacidosisis or lactic acidosis or antifreeze or vomiting.
Compensated quickly by ventilation

54
Q

Describe acute effects upon ventilation of falling pO2, increase in inspired pCO2 and falls in arterial plasma pH.

A

All increase

55
Q

Location and function of central chemoreceptors. Roles if the cerebrospinal fluid (CSF) blood brain barrier and choroid plexus in the response

A

Medulla around CSF. Detect pH only affected by CO2 which freely diffuses but HCO3 does not. If increaesed/ decreased ventilation does not solve then HCO3 diffuse via choroid plexus to neutralise and stop.

56
Q

Metabolic acidosis detection?

A

Peripheral as only change I’m HCO3??

57
Q

Describe type 1 resp failure

A

Low O2 but normal or decreased CO2.
Occurs when problems in ventilation/perfusion or diffusion barrier. E.g. Pneumonia, PE
Breathlessness, central cyanosis, exercise intolerance

58
Q

Describe type 2 resp failure

A

Low O2 me high Co2.
Problems with ventilation e.g. Chest wall probs, COPD, asthma, opioids
Acutely then breathlessness but compensation occurs and CSF equilibriates so driven by hypoxia. Can cause pulmonary hypertension due to contraction in response to hypoxia

59
Q

How can arterial blood gases be measured?

A

Pulse oximetry

60
Q

Describe ventilation/perfusion mismatch and diffusion impairment and how they can lead to type1. Outline the causes of each

A

Want to be 1 (0.8 is normal).

PE/ thicker barrier (pneumonia) means less perfusion so not all O2 breathed off

61
Q

Describe how hypoventilation results in type 2 and outline its important causes

A

Fibrotic lung disease, COPD, emphysema (severe), severe asthma, scoliosis/ kyphosis

62
Q

Define asthma and describe the nature of airflow obstruction in asthma

A

Chronic disease characterised by airway remodelling - thickening of SM and BM. Reversible airflow obstruction. Hypersensitivity/ increased airway responsiveness to a variety of stimuli.

Damaged epithelium due to chronic inflammation

More likely in females. Can be allergic (eosinophils, IgE and mast cells), asprin sensitive or occupational (farmers, welders and bakers)

63
Q

Describe the pathophysiology of asthma

A

Mucins and hypersensitivity/ contraction and narrowing of airway make a reversible airflow obstruction.
To maintain flow pressure must change (r4) (poiseuilles equation)

64
Q

Describe the precipitating factors for asthma attack

A

ACh release- muscurinic agonist, prostaglandins, leukotrienes, histamine, cold air

Allergens - dust mites, air pollution, fungal spores, HDM, pollens

65
Q

Describe the signs and symptoms of asthma and their physiological basis

A 
Dry cough- no infection- worse on exercise
Respiratory wheeze
Dispnoea 
Chest tightness
Recession and tracheal tug
Prolonged expiratory phase
66
Q

Describe the tests used to assess the condition of a patient suspected of asthma and how they are interpreted

A

History- eczema, family history, prenatal smoking, occupation
Examination- hyperesonant, barrel chest,
Investigation- flow volume loop- restrictive, auscultation polyphonic wheeze.

lower FEV/FVC or normal, lower PEFR- 12% increase in FEV with salbutamol. bronchial hyper responsiveness- bronchial challenge test e.g, histamine.
FENO- released from inflammation.
Allergy testing
Sputum induction
Exercise induced bronchoconstriction- pre and post spirometry.

67
Q

Principles of treating asthma

A

Prevent- smoking, allergens, exercise, housing, cleaning
B2 agonists
Muscurinic antagonists -ipratropium (anticholinergic)
Theophylline/ aminophylline (anti inflam)
Corticosteroids and leukotrienes receptor antagonist .
Acutely- IV drugs, interbate, ventilate, salbutamol and atrovent nebs, O2

68
Q

Peripheral chemoreceptors location

A

Carotid and aortic bodies

69
Q

Describe the major precipitating factors for asthmatic attacks

A

Lack of treatment adherence
Respiratory virus infections associated with the common cold
Exposure to allergen or triggering drug e.g. NSAIDS

70
Q

Describe the main causes of COPD and the nature of airflow obstruction in COPD

A

Chronic bronchitis - inhaled irritants e.g. Smoking, cause chronic inflammation which damages muco-ciliary escillator, damages epithelium, increases mucous secretion with the result being narrowed airways
Emphysema - loss of elastin leading to destruction of alveolar walls, irritants and inflammation
Both are progressive and not fully reversible

71
Q

Describe the signs and symptoms of COPD

A

Tachypnoea
Cough dry or productive worse at night
Infection
Barrel chest, hyper resonant due to hyperinflation and air trapping
Leaning forward- accessory muscles
Reduced intensity breath sounds
Reduced air entry, loss of elasticity and tissue breakdown increasing resistance and residual capacity.
Possible wheeze
May develop pulmonary hypertension, central cyanosis, Hypercapnia (flapping tremors.
MRC Dyspnoea scale

72
Q

Investigations of COPD patients

A

Cxr- hyper expansion - flat diaphragm, more than 6 ribs, increased anteroposterior diameter, hyperlucent lungs, signs of pneumonia/ pneumothorax, rule out other stuff.
Pulse oximetry and ABG
Lung function tests- ratio under 70% and limited reversibility. Reduced FEV

73
Q

Management of COPD patients

A

ACh blockers Ipratropium, bronchodilators- salbutamol.
Stop smoking
Exercise
Education
Surgery- remove bullae from emphysema, lung transplant,
Pneumonia vaccine
Oxygen therapy- prevent hypertension and relieve symptoms (not if breathless) long as possible, portable or just intermittent
Corticosteroid- decrease inflammation
Ventilate
Pulmonary rehab- increase exercise capacity

74
Q

Outline normal flora of the GI tract

A

Viridens streptococci (a haemolytic), anaerobes, neisseria spp, Candida albicans
Sometimes:
Strep pneumoneai, pyrogens, h influenzae,
Rare:
E. coli, pseudomonas

75
Q

Natural defenses of respiratory tract against infection

A

Muco ciliary escalator
Lymphatics, alveolar macrophages, IgA and IgG secreted
Cough and sneeze

76
Q

Main infectious diseases of upper respiratory tract and the organisms commonly causing these infections

A 
Sinusitis
Parotitis
Tracheitis 
Laryngitis 
Pharyngitis 
Otitis media
Rhinitis - cold
Epiglottitis

RSV
Coronovirus
Influenza
Rhinovirus

May lead to bacterial infection
Meningitis
Mastoiditis
Brain abcess
Common with sinusitis or Otitis media
77
Q

Define the term pneumonia and distinguish between acute and chronic

A

Pneumonia- infection of lung parenchyma with consolidation (not compressible) and exudate
Acute/ lobar- one lobe affected normally CA and strep pneumoniae. May lead to emphyma, lung abscess or bronchiectasis (widened)
Chronic - bronchial- multiple lobes affected, widespread/ patchy consolidation, starts in bronchi, often hospital aquired, may cause heart failure, viral infections.

78
Q

Describe the infectious aetiology of acute community acquired and acute hospital aquired pneumonias

A

Ca:
Common- strep pneumoniae, Haemophilus influenza, klebsiella pneumoniae
Atypical- chlamydia pneumophila, mycobacterium pneumoniae, legionella pneumophila
Viral- influenza, RSV
Ha- staph aureus, E. coli, pseudomonas aeriginosa,
Immunosupression- pneumocystis jirovecii, candida, aspergillus, viruses

79
Q

List the aetiological clues for the common respiratory tract pathogen

A 
Strep pneumoniae- elderly, co morbid
Aspiration - E. coli
Legionella- travelling
H influenzae - COPD
Mycoplasma- young, prior antibiotics, extra pulmonary involvement
S aureus- drug user, post viral
80
Q

Clinical features of pneumonia

A 
Malaise
Fever
Cough- productive, can vary in sputum
Dyspnoea
Chest pain on inspiration
Chills, sweats rigors 
Vomiting
Anorexia 
Myalgia
Diarrhoea 
Wheeze

Dull on percussion
Ausculation- crackles, wheeze, bronchial breath sounds

81
Q

Investigations of pneumonia

A

CXR

Culture/ labs see other card

82
Q

How do you assess the severity of pneumonia/ management?

A 
Confusion
urea >7
Resp rate over 30
Blood pressure  less than 90 or 60
65 +
2+ = hospital
3+ = ICU
83
Q

Understand the principles of collection of specimens for lab diagnosis of pneumoniae

A 
Nose/ throat swab
Sputum sample- bronchial/alveolar lavage
Biopsy?
Blood
Urine- legionella
Serotyping

Microscopy
Macroscopic - sputum
Culture- stain acid and alcohol fast
Antibody/ antigen detection

84
Q

Common opportunistic pneumonia infections

A

Pneumocystis spp.
Aspiration e.g. Coma, alcoholics, epilepsy, dysphagia - E. coli and pseudomonas
Whooping cough- bordetella pertussis- culture and PCR, cough and vomit, erythromycin
Aspergillus and candida
Cytomegalovirus
Cryptosporidium Protozoa
Mycobacterium spp.
CF- haemophilus, s aureus, later pseudomonas auringinosa.

85
Q

Describe the principles of anti microbial therapy in pneumonia and understand the rationale for selecting different antibiotics

A

Pneumococcus- amoxicillin or if severe then co-amoxiclav

If atypical then erythromycin,clarithromycin, doxycycline, levofloxacin for legionella.

86
Q

Describe the microbiology of mycobacterium tuberculosis

A

Acid and alcohol fast bacilli.

Spread via aerosol

87
Q

Describe the pathology of m tuberculosis

A

Acute- forms primary complex- sub pleural lesions Ghon’s focus and infects hilar lymph nodes. When they occur together they are called the primary complex. Can calico fly or spread.
Post primary infection - beyond first week, throughout body/ lung military spread. Cavitation of lungs and cytokines mediated systemic effects.
Spread to kidneys, limbo sacral spine, large joints, meningitis.

88
Q

Describe the host response to a TB infection

A

Ingested by macrophage but prevents fusion of phagosome with lysosomes.
Escapes and multiplies in cytoplasm.
Provokes immune response - il2 then IFn-g and TNF a. Activate and recruit more macrophages causing granulomas

89
Q

Describe the typical presentation and radiographic changes in resp TB

A 
Dyspnoea
Cough- wet or dry
Haemoptysis
Fever
Primary - asymptomatic 
Tiredness and malaise
Weight loss and anorexia.

Non specific signs, palor, fever, weigtloss, clubbing, lymph nodes
X ray changes - shadowing, cavities, consolidation, military seeds, Cardiomegaly, calcification.

90
Q

Describe the primary and post primary changes in TB

A

Primary - swollen lymph possible

Post primary - symptoms especially cough, fevers and weight loss.

91
Q

Describe lymph TB

A

Affects neck- internal thoracic, swollen, inflamed, may compress trachea/ bronchi

92
Q

Describe orthopaedic TB

A

Spondylitis- sub chondral ossification along lateral ligaments - paraplegia and quadriplegia possible
Poncets disease- poly arthritis

93
Q

Describe meningitis from TB

A

Headache, fever, confusion coma.

Normally from military TB

94
Q

Describe pleural TB

A

Hypersensitivity response in primary infection
Or
Tuberculous Empyema with ruptured cavity through chest wall.

95
Q

Describe miliary TB

A

Bacilli in blood from primary or reactivation.

Spread to multiple organs/ sites within lungs.

97
Q

Diagnosis of TB

A

Clinical features
CXR
Sputum sampling- swab/ lavage, blood culture, biopsy

97
Q

Describe the mechanisms of drug resistance in TB

A

Spontaneous mutations.

Poor adherence means multi drug resistant TB (mdrtb) increasing.

98
Q

Describe the management of TB and side effects

A

Rifamipicin- hepatitis, rash, flu like symptoms, ARF, thrombocytopenic purpura
Isoniazid- hepatitis, rash, peripheral neuropathy
Pyrazinamide - hepatitis, rash, arthralgia
Ethambutol- optic neuritis
4 then 2 2 months and 6 months
Only infectious for 2 weeks
Poor adherence

99
Q

Describe the BCG

A

Uses live attenuated bovine tuberculosis bacillus. Lasts 15 years. Variable efficacy.
Used for high risk groups

100
Q

High risk groups TB

A 
HIV
Corticosteroids or anti TNF antibody
Immunosuppressant 
Post surgery
Silicosis
Malnutrition 
IV drug
Overcrowding 
Smokers and chronic lung disease
Asians
Diabetes
101
Q

Describe the relationship between TB and HIV

A

Leading cause of death in HIV patients.

Much higher risk

102
Q

Describe public health issues surrounding a case of TB

A

Immediate contact with TB radiology if suspected and treatment started immediately

103
Q

Describe the incidence of lung cancer in different groups

A

Men 100 in 100000 mortality vs 40 in women
Linked to socioeconomic factors
Increasing in women and decreasing in men

104
Q

Give an account of the aetiological factors involved in lung cancer

A 
Smoking - most 
Radon
Genetics
Asbestos 
Diet
105
Q

Describe the typical pattern of symptoms reported by patients with lung cancer

A

Primary- Haemoptysis, Dyspnoea, cough, chest pain, wheezing, post obstructive pneumonia
Regional mets- hoarseness, Dyspnoea - phrenic nerve, SVC obstruction, dysphagia
Distant mets - bone pain fractures, CNS features, vision, headache, confusion ect.
.

106
Q

Where can lung cancer spread?

A

Brain, lymph, pericardium, lung, pleura. Liver, adrenals, bone

107
Q

Describe common paraneoplastic syndromes associated with lung cancer and understand the structural abnormalities underlying them

A

Paraneoplastic- endocrine cushings,SIADH, hypercalcaemia
Neurological - encephalopathy, peripheral neuropathy, eaton-lambert syndrome
Anaemia, thrombocytosis, clubbin

108
Q

Common methods used to obtain material for histological diagnosis

A

Histological diagnosis necessary for cell type and prognosis
Bronchoscopy
Needle biopsy
Thoracocentesis

109
Q

Diagnosis and staging of lung cancer

A

Initially CXR
Serum biochemistry
Imagining with ct, isotope bone scan, bronchoscopy
Tissue with biopsy

110
Q

Give an account of he histology and classification of common lung tumours

A

Non small cell:
Squamous cell carcinoma (40%) - central angulate cells, eosinophilic, keratinisation (pearls)
Adenocarcinoma 35%- peripheral tumours, columnar/ cuboidal cells, acini, papillary structures, May line alveoli, may produce mucins
Large cell carcinoma
Small cell carcinoma 12%- less cytoplasm, small nuclei, nuclear moulding, necrosis and mitosis. Oat cell carcinoma

111
Q

Behaviour of different cancer and prognosis and treatment

A

Most non small cell are inoperable but most small cell are metastatic so has a worse prognosis.

112
Q

Different treatments for lung cancer

A

Surgery for NSS
Chemotherapy, potentially curative in NSS and can lead to improvements in SS
Radiotherapy- radical or palliative
Biological therapies- EGFR, immunotherapy
Combination therapy
Palliative care

113
Q

Describe pleural effusion, pneumothorax, consolidation, space occupying lesion, lung collapse

A

Pneumothorax- black air trapped, visible pleural edge, tracheal shift away
Pleural effusion- loss of costs phrenic angles of hemidiaphragm, meniscus of fluid
Consolidation- dense opacification
SOL- nodule less than 3, mass larger. Causes malignancy, inflammation, congenital, benign mass legion
Lung collapse- elevation of hemidiaphragm, crowding of ribs, shift of mediastinum towards, crowding of pulmonary vessels, sail sign

114
Q

Identify cardiac enlargement/ cardiac index

A

PA

Ratio of heart to rib age at largest. Normal is below 50%

115
Q

Causes of ILS

A

Immunological - sarcoidosis- steroids, may be obstruction too
Connective tissue disorder- RA, SLE, scleroderma, polymyositis
Occupational- coal workers, farmers - extrinsic allergic alveolitis e.g. Bird fanciers lung, farmers, asbestososis
Idiopathic (50%)- IPF steroids, IIP no treatment
Treatment related- methotrexate, amioderone, nitroflurotoin, chemotherapy

116
Q

Describe the involvement of different inflam cells in interstitial lung disease

A

Area inbetween air spaces for support, diffusion and repair

Epithelial, endothelial, macrophages, mesenchymal and other inflam cells

117
Q

Clinical features of ILS.

A

SOB, reduced exercise tolerance, dry cough
Tachpnoea, tachycardia,reduced chest movements, coarse crackles, cyanosis, RHF, clubbing in CFA(crypto genic fibrosing alveolitis)
Restrictive

118
Q

Effect on gas exchange

A

Reduced transfer factor
Fibrosis so dead space
Less compliance
Increased diffusion pathway

119
Q

Lung function tests of ILS

A

Restrictive so decreased FVC

120
Q

Lung diseases and occupations ILS

A

Diffuse fibrosis- asbestosis is
Modular fibrosis- pneumoconiosis, duct, silica, asbestos
Alveolitis- farmer, pigeon

121
Q

Xray of ILS

A

Fibrosing alveolitis - small, micro modular shadowing, ragged heart boarder
Extrinsic allergic alv - acute micro nodules, chronic is almost normal then disease
Sarcoidosis- military modular shadowing, diffuse fibrosis
Asbestosis is- plaques, fibrosis, mesothelioma

122
Q

Factors affecting formation and reabsorption of pleural fluid

A

Production of absorption failure
Production- increase in pressure, increase in interstitial fluid, increase in permeability e.g. Infection or malignancy, decrease in oncotic
Absorption- increase in BP, lymph blockage

123
Q

Types of pleural effusion

A

Haemothorax
Chylothorax (lipid)
Empyema (pus)
Simple effusion (serous fluid)

124
Q

Transudate / exudate

A

30g/litre
Transudate- difference in starling forces
Exudate- dilation or vasculature or leakage

125
Q

Describe the characteristics and causes of pleurisy

A 
Chest pain- if diaphragm then shoulder
Pain on inspiration, cough, sneeze, laugh
Small breaths
Pleural rub can be heard
Causes
Autoimmune - RA, SLE
Infection
Cancer- mesothelioma (asbestos) 
Pneumothorax
PE
Unabsorbed effusion Can lead to pleural fibrosis
126
Q

Describe chest wall abnormalities and motor/ neurological diseases that can affect breathing

A

Pertussis carcinatum and excavatum, kyphosis, scoliosis. Acquired deformities. Muscular dystrophy, Motor neurone disease, polio

127
Q

Course of the oblique fisssures

A

T2 SP- anterior behind 6 costal cartilage

128
Q

Course of the right horizontal fissure

A

4th rib from MAL to anterior edge

Esa 3 (5 decks)

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